Open Access

ARTICLE

Effects of tumor necrosis factor antagonist treatment on hepatitis C-related immunological abnormalities

Christelle Vauloup¹, Roman Krzysiek^1,2, Liliane Greangeot-Keros¹, Daniel Wendling³, Phillippe Goupille⁴, Rachel Brault⁵, Christine Brousse⁶, Xavier Mariette⁷, Dominique Emilie^1,2

1 Service de Microbiologie-Immunologie Biologique, hôpital A. Béclère, Assistance Publique-Hôpitaux de Paris
2 INSERM 764, Institut Paris-Sud Cytokines, Université Paris-Sud, 157 Route de la Porte Trivaux, 92140 Clamart, France
3 Service de Rhumatologie, Centre Hospitalo-Universitaire de Besançon, 25030 Besançon, France
4 Service de Rhumatologie, hôpital Trousseau, 37044 Tours, France
5 Service de Rhumatologie, hôpital de la Mileterie, 86021 Poitiers, France
6 Service de Rhumatologie, hôpital Foch, 92150 Suresnes, France
7 Service de Rhumatologie, hôpital de Bicêtre, Assistance Publique-Hôpitaux de Paris et INSERM E109, Université Paris-Sud, 94275 Le Kremlin-Bicêtre, France

* Corresponding Author: D. Emilie,

European Cytokine Network 2006, 17(4), 290-293. https://doi.org/10.1684/ecn.2006.0046

Abstract

Background. Chronic hepatitis C infection is frequently associated with a mixed cryoglobulinaemia and circulating auto-antibodies, especially anti-smooth muscle cells (SMA) and anti-liver/kidney/microsome type 1 (LKM-1) anti-tissue antibodies. Treatments with TNF antagonists favour the emergence of auto-antibodies, and particularly anti-dsDNA antibodies. Objective. To determine the impact of TNF antagonists on hepatitis C-related immune abnormalities. Methods. We prospectively monitored for 14 weeks, six patients with actively replicating chronic hepatitis C, initiating an anti-TNF treatment for an associated rheumatoid arthritis. Results. Anti-nuclear and anti-dsDNA antibodies were induced in two and three patients, respectively. Treatment had no impact on the production of antibodies against extractable nuclear antigens, and it did not induce anti-tissues antibodies in any patient. Cryoglobulinaemia appeared in 2/6 patients, and it persisted in 2 others. No patient developed any news signs of autoimmunity. HCV viraemia remained unchanged. Conclusions. Induction of auto-antibodies by TNF antagonist treatments does not involve anti-tissues antibodies, even in patients with actively replicating chronic hepatitis C prone to produce anti-SMA and anti-LKM-1 antibodies. In contrast, TNF antagonists may favour emergence of cryoglobulinaemia in such patients.

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